Evidence map›Paper›PMID 42485309›Full record

ArticlePloS one2026

Molecular signature of COVID-19 prior to its exacerbation by multi-omics survey.

Tomoyuki Suzuki, Yoshihiro Kita, Keisuke Yanagida, Kenji Maeda, Tomomi Hashidate-Yoshida, Hiroki Nakanishi, Takayo Ohto-Nakanishi, Junko Terada-Hirashima, Yoshie Tsujimoto, Masayuki Hojo and 3 more

Abstract read
In one paragraph

Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Tomoyuki SuzukiDepartment of Lipid Life Science, National Institute of Global Health and Medicine, Japan Institute for Health Security, Tokyo, Japan.
Yoshihiro KitaLife Sciences Core Facility, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Keisuke YanagidaDepartment of Lipid Life Science, National Institute of Global Health and Medicine, Japan Institute for Health Security, Tokyo, Japan.ORCID https://orcid.org/0000-0002-4092-1416
Kenji MaedaDivision of Antiviral Therapy, Joint Research Center for Human Retrovirus Infection, Kagoshima University, Kagoshima, Japan.
Tomomi Hashidate-YoshidaDepartment of Lipid Life Science, National Institute of Global Health and Medicine, Japan Institute for Health Security, Tokyo, Japan.
Hiroki NakanishiLipidome Lab Co., Ltd., Akita, Japan.
Takayo Ohto-NakanishiDepartment of Lipid Life Science, National Institute of Global Health and Medicine, Japan Institute for Health Security, Tokyo, Japan.
Junko Terada-HirashimaDepartment of Respiratory Medicine, National Center for Global Health and Medicine, Japan Institute for Health Security, Tokyo, Japan.
Yoshie TsujimotoDepartment of Respiratory Medicine, National Center for Global Health and Medicine, Japan Institute for Health Security, Tokyo, Japan.
Masayuki HojoDepartment of Respiratory Medicine, National Center for Global Health and Medicine, Japan Institute for Health Security, Tokyo, Japan.
Hiroaki MitsuyaDepartment of Refractory Viral Diseases, National Institute of Global Health and Medicine, Japan Institute for Health Security, Tokyo, Japan.
Takao ShimizuDepartment of Lipid Life Science, National Institute of Global Health and Medicine, Japan Institute for Health Security, Tokyo, Japan.
Hideo ShindouDepartment of Lipid Life Science, National Institute of Global Health and Medicine, Japan Institute for Health Security, Tokyo, Japan.ORCID https://orcid.org/0000-0002-3443-913X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused a global pandemic due to its high transmissibility and ability to evade innate immune responses. Comprehensive characterization of the disease is essential for elucidating its pathophysiology and clinical progression. In this study, we performed multi-omics analyses of plasma samples collected from SARS-CoV-2-positive patients prior to clinical deterioration of coronavirus disease 2019 (COVID-19). These samples revealed the potential of previously reported clinical parameters, including CRP and neutrophil level, to predict COVID-19 exacerbation in the early stage. Our analysis identified a novel panel of molecules that precede the clinical manifestations associated with COVID-19 progression. These candidate biomarkers exhibited strong correlations with previously reported clinical and immunological parameters. Notably, several inflammation-related markers showed inverse associations with specific interferon subtypes, including IFN-α6 and IFN-α8, potentially reflecting mechanisms of SARS-CoV-2-mediated immune evasion. Our findings contribute to the understanding of virus-induced acute exacerbation and offer a valuable foundation for future pandemic research.

Indexed as

COVID-19SARS-CoV-2BiomarkersDisease ProgressionHumansMultiomicsBiomarkers

Identifiers

PMID42485309
PMCPMC13390879

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.